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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The usually accepted risk factors for late post-traumatic seizures (LPTS) are those identified years ago by Jennet: early post-traumatic seizure (EPTS), depressed fracture, intracranial haematoma. Prolonged unconsciousness (PTA greater than 24 hrs) is another factor usually added. More recently, personal experience of the Authors and the data of the literature, compel us to question the validity of known risk factors based on clinical data. Authors believe that the identification of patients at risk for LPTS depends mainly on the precise definition of trauma severity and on CT or surgically documented lesions of brain substance. Three groups of patients, characterized by the presence of one or more of the accepted risk factors of LPTS, have been studied. In our experience, while in adults the presence of documented cortico-subcortical lesions represents the main risk factor of LPTS, in children the appearance of EPTS per se increases the risk of LPTS, irrespective of the presence of documented brain lesions. Alteration of consciousness without a focal lesion, even if prolonged and severe, is not a risk factor for LPTS.
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PMID:Risk factors for late posttraumatic epilepsy. 141 48

A 73-year-old man was admitted with gait disturbance and dysarthria. He showed right-side cerebellar ataxia. Computed tomography of brain showed left thalamic bleeding. Nine months later, he was admitted again because of seizure and consciousness disturbance. He had a history of diabetes mellitus and gout for five years, but no hypertension. On physical examination the lungs and heart were normal. On neurological examination, he showed stupor,pupils and eye position were normal. He showed right hemiparesis and urinary incontinence. The deep tendon reflexes were (+) at the upper limbs and (2+) at the right knee and ankle. Blood pressure was 162/88 mmHg and glucose was 275 mg/dl. Other laboratory data were normal. Brain CT showed hemorrhage of the left frontal lobe. The cystatin C level in cerebrospinal fluid was 68 ng/ml. Therefore we suspected cystatin C deposit amyloid angiopathy. In this case, thalamic hemorrhage was initially thought to be amyloid angiopathy. In cases of cerebral hemorrhage in the elderly without hypertension, we must be considered amyloid angiopathy.
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PMID:[A case of recurrent cerebral hemorrhage considered to be cerebral amyloid angiopathy by cerebrospinal fluid examination]. 143 57

We reported a case with sequelae of SMON and painful tonic seizure (PTS). The patient was a 50-year-old woman. Onset of SMON was when she was 28 years old. She has been suffering from decreased sensation and dysesthesia below C8 cord level to a severe degree, gait disturbance to a moderate degree and visual disturbance to a slight degree. Since January 1990, she experienced stereotyped tonic seizures of all extremities and trunk without consciousness disturbance, preceded by tingling sensation ascending from bilateral distal legs, several times a day. During hospitalization, epilepsy, tetany and multiple sclerosis were ruled out and its seizures were completely depressed by oral administration of a small amount of carbamazepine. PTS which is said to be characteristic of multiple sclerosis is seldom found in SMON patients. This is a very important and interesting case to suggest a certain relation between the mechanism of PTS and the cord lesions of SMON.
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PMID:[A case report of a patient with sequelae of SMON and painful tonic seizure]. 176 54

It has been known that various derangements in ionic homeostasis develop following neural trauma. In particular, potassium efflux out of and calcium influx into the cells are thought to play important roles in causing cell damage. Concomitantly we have previously reported that increased extracellular potassium per se provoked by head injury induces convulsive seizure such that the sustained high extracellular potassium leads to animal death. The purpose of the present study was further to examine the beneficial effect of drugs which could inhibit such detrimental ion movements in experimental head injury. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 gm dropped from a height of 17.6 cm above the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in about 70% and death in about 30% of animals. The severity of consciousness disturbance was evaluated by a pair of indices in time interval; time required for the recovery of righting reflex (RR) and for the recovery of spontaneous movement (SM). Ethacrynic acid, a loop diuretics, blocks carrier-mediated chloride transport into astroglia associated with sodium and water in the presence of high extracellular potassium. Animals were treated with either 0.5-1.0 mg/kg or 2.0-4.0 mg/kg of ethacrynic acid administered via tail vein 10 min before injury. In the other group of animals, a calcium entry blocker, flunarizine was injected intraperitoneally in doses 5, 10 and 20 mg/kg one hour pre-insult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Protective effect on the brain of ion-blockers in experimental head injury]. 243 80

Complications following the operations for chronic subdural hematoma include recurrence of the hematoma, infection, seizure, and failure of the brain to expand due to cerebro-cranial disproportion. This report presents cases with intracerebral hemorrhage which is relatively rare complication. In case 1, a 35-year-old man developed status epilepticus immediately after the operation for chronic subdural hematoma. An emergency CT scan revealed acute brain swelling, and still, after the external decompressive craniotomy, CT scan showed severe brain swelling with subcortical diapedetic hemorrhage. In case 2, a 78-year-old woman whose CT scan had shown bilateral CSH and brain herniation, demonstrated intracerebral hemorrhage in the medial occipital lobe when examined post-operatively by CT scan. It is possible that the mechanisms of intracerebral bleeding following the operation for CSH are 1) diapedesis through increased permeability of parenchymal blood vessels due to the sudden increase in cerebral blood flow following the existence of longstanding extracerebral mass, and 2) hemorrhagic infarction due to recanalization of posterior cerebral artery compressed by the herniating medial temporal lobe. We should therefore avoid sudden decompression in the management of the cases which showed pre-operative consciousness disturbance or abnormal low or high density on CT scan, because these findings may be preoperative indications of brain fragility.
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PMID:[Intracerebral hemorrhage immediately following the operation of chronic subdural hematoma]. 268 37

Clinical and pathological studies were made on 5 patients (1 male and 4 females; average age, 58.2 years) with primary malignant lymphoma of the brain. One case had received long-term immunosuppressive therapy for SLE. The most common initial signs and symptoms were non-specific and non-localized. They included headache, disorientation and consciousness disturbance. During the course, the signs and symptoms consisted of consciousness disturbance (5 cases), hemiparesis (4 cases), headache (3 cases), dementia (2 cases), seizures (2 cases), and diplopia (1 case). The tumors on CT scans appeared as slight hyperdense areas in 3 cases, and as isodense areas in 1 case with enhancement following contrast media infusion, which was compatible with previously reported results. However, the other case showed diffuse hypodense areas without enhancement which has rarely been reported. Multiple lesions were found in 4 cases. Three cases underwent cerebral angiography which demonstrated avascular masses. Pathologically, the tumors were located in the cerebral hemispheres in 5 cases, the basal ganglia and thalamus in 3 cases, the brain stem in 2 cases, and the cerebellum in 2 cases. Three cases were classified as of the diffuse, large cell type, 1 case as small cleaved cell and 1 case as immunoblastic. Thus, the clinical diagnosis of primary malignant lymphoma of the brain still remains difficult because the symptoms and CT findings are so varied.
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PMID:Primary malignant lymphoma of the brain--clinical and pathological investigations. 272 42

In order to clearing the influence of neurotransmitters in concussive unconsciousness, immediate convulsion and mortality, the following experiments were performed. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 gm dropped from a height of 20 cm on to the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in 66% and death in 30% of animals. The severity of consciousness disturbance was evaluated by two parameters; (1) time interval required for the recovery of righting reflex (RR) and (2) time interval for the recovery of spontaneous movement (SM). Agonist or antagonist of various neurotransmitters was given intraperitoneally 0.5 or 2 hours before injury. The following results were obtained although some of them were statistically not significant. Physostigmine shortened both RR (p less than 0.1) and SM (p less than 0.01), whereas scopolamine did not change these intervals. Atropine sulfate shortened both of them. Nevertheless, atropine methylbromide, which dose not pass through blood-brain-barrier, also had same effects. Methamphetamine shortened both RR (p less than 0.1) and SM (p less than 0.05), whereas haloperidol prolonged these intervals. 5-HTP shortened RR (p less than 0.05), but prolonged SM (p less than 0.1). Methysergide shortened both RR (p less than 0.05) and SM (p less than 0.01). Convulsive seizure was suppressed by physostigmine (p less than 0.01) or 5-HTP (p less than 0.20). These results suggested that suppression of dopaminergic and cholinergic systems, and/or activation of serotonergic system contribute to concussive unconsciousness.
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PMID:[The influences of neurotransmitters on the traumatic unconsciousness, immediate convulsion and mortality in the experimental mice model]. 289 33

In West Germany, the antihistaminic diphenhydramine is marketed as a non-prescription hypnotic. Results of toxicological screening in cases of drug overdose indicate that poisoning with diphenhydramine represents a substantial part (4.5%) of the total number of intoxications. A total of 136 cases of diphenhydramine poisoning in 1982-1985 were evaluated with respect to age, ingested dose, plasma level, and clinical symptomatology. All patients had taken diphenhydramine with suicidal intent. Two-thirds of the patients were aged 14-30 years. In about 50% of the cases, between 6 and 40 times a therapeutic dose was ingested. Diphenhydramine plasma levels showed a wide range (0.1-4.7/micrograms/ml) due to differences in ingested dose and time between ingestion and admission to hospital. Impaired consciousness was the most common symptom. Psychotic behavior similar to catatonic stupor--often combined with anxiety--was highly specific for diphenhydramine poisoning. Further symptoms included hallucinations, mydriasis, tachycardia, and less frequently diplopia, respiratory insufficiency, and seizures. Primary treatment included gastric lavage, administration of activated charcoal and sodium sulfate. In one case, hemodialysis and ultrafiltration were performed which had only limited effect on diphenhydramine plasma elimination kinetics. This patient died of diphenhydramine overdose and extreme hypothermia. All intoxications except the one mentioned before had an uncomplicated clinical course. In vitro experiments indicate that diphenhydramine may be almost completely removed from the plasma compartment by hemoperfusion. Routine analysis of urine samples in diphenhydramine overdose led to the identification of 4 previously unknown metabolites and artifacts of diphenhydramine.
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PMID:Clinical symptomatology of diphenhydramine overdose: an evaluation of 136 cases in 1982 to 1985. 358 86

Despite the widespread use of glucocorticoids in patients with severe head injury, the usefulness is still controversial. In the past, the effect was investigated only in terms of dose-response relationship. We have, however, studied the time factor for the administration of dexamethasone to obtain maximal beneficial effect together with investigating the influence of actinomycin-D, an inhibitor of messenger RNA synthesis, before dexamethasone treatment. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 g dropped from a height of 17.8 cm above the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in about 70% and death in about 30% of animals. The severity of consciousness disturbance was evaluated by a pair of indices in time interval: time required for the recovery of righting reflex (RR) and for the recovery of spontaneous movement (SM). 4 mg/kg of dexamethasone phosphate was given intraperitoneally 0.5, 4, 6, 12, 18 or 24 hours before injury. Actinomycin-D of 0.5 mg/kg was injected intravenously 1 h before each dexamethasone treatment in separate animals. In the other group of animals, dose was changed with varying time course of dexamethasone pretreatment, e.g., 2, 4, 6 or 8 mg/kg given 0.5, 2 or 4 h before injury. It was found that dexamethasone of 4 mg/kg pretreatment 4-12 hours significantly improved the recovery from consciousness disturbance and death rate. Actinomycin-D given before dexamethasone treatment completely abolished the protective effect of dexamethasone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Time course of the cerebroprotective effect of dexamethasone in experimental head injury]. 382 51

A patient is described who developed unilateral seizures whilst being treated with recombinant interferon for hairy cell leukemia. Special features included the relatively low dose of interferon, the focal aspect of the epilepsy and the high resistance to anticonvulsants. Oligoclonal banding of cerebrospinal fluid proteins may have resulted from polyclonal activation of bone marrow plasma cells during interferon treatment. Disturbances of consciousness, dysphasia, visual hallucinations, upper motor neuron deficit, tremor, dizziness, numbness, myalgia and headache, all of them neurological complications of interferon treatment, are discussed.
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PMID:Unilateral seizures in a patient with hairy cell leukemia treated with interferon. 393 49


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